EasySep™小鼠上皮细胞富集试剂盒II

免疫磁珠负选

产品号 #19868

免疫磁珠法分离未标记的小鼠上皮细胞

产品优势

  • 快速、易于操作,且无需分离柱/li>
  • 分选得到的细胞未被标记

产品组分包括

  • EasySep™小鼠上皮细胞富集试剂盒II(产品号#19868)
    • EasySep™小鼠上皮细胞富集抗体混合物,0.5mL
    • EasySep™生物素分选抗体混合物,1mL
    • EasySep™ Dextran RapidSpheres™磁珠,1mL

概述

EasySep™ 小鼠上皮细胞富集试剂盒II专为通过免疫磁珠负选法从新鲜解离的小鼠乳腺组织中分离上皮细胞而设计。该试剂盒通过使用生物素标记的抗体复合物和磁珠标记非目的细胞。通过EasySep™磁极将被磁珠标记的细胞与未被标记的目的细胞分离,接着简单地将目的细胞倾倒或吸取至一个新的分离管中。该产品可替代EasySep™人EasySep™上皮细胞富集试剂盒(产品货号#19758)以进行更快的细胞分选。同时也可替代EasySep™ 小鼠乳腺干细胞富集试剂盒(产品货号#19757)中的细胞富集部分。

MAGNET COMPATIBILITY
• EasySep™ Magnet (Catalog #18000)
• “The Big Easy” EasySep™ Magnet (Catalog #18001)
 
SUBTYPE
Cell Isolation Kits
 
CELL TYPE
Mammary Cells, Prostate Cells
 
SPECIES
Mouse
 
SAMPLE SOURCE
Other, Primary
 
SELECTION METHOD
Negative
 
APPLICATION
Cell Isolation
 
BRAND
EasySep
 
AREA OF INTEREST
Epithelial Cell Biology

实验数据

Starting with mouse mammary tissues, the epithelial cell content of the enriched fraction is typically 96.97 ± 0.54% (mean ± SD using the purple EasySep™ Magnet). In the above example, the percentages of epithelial cells in the start and final enriched fractions are 19.9% and 97.4%, respectively.

产品数明书及文档

Find supporting information and directions for use in the Product Information Sheet or explore additional protocols below.

Document Type
Product Name
Catalog #
Lot #
Language
Catalog #
19868
Lot #
All
Language
English
Document Type
Safety Data Sheet 1
Catalog #
19868
Lot #
All
Language
English
Document Type
Safety Data Sheet 2
Catalog #
19868
Lot #
All
Language
English
Document Type
Safety Data Sheet 3
Catalog #
19868
Lot #
All
Language
English

应用领域

This product is designed for use in the following research area(s) as part of the highlighted workflow stage(s). Explore these workflows to learn more about the other products we offer to support each research area.

相关材料与文献

Educational Materials (4)

Publications (2)

Sterol regulatory element binding protein 1 couples mechanical cues and lipid metabolism. R. Bertolio et al. Nature communications 2019

Abstract

Sterol regulatory element binding proteins (SREBPs) are a family of transcription factors that regulate lipid biosynthesis and adipogenesis by controlling the expression of several enzymes required for cholesterol, fatty acid, triacylglycerol and phospholipid synthesis. In vertebrates, SREBP activation is mainly controlled by a complex and well-characterized feedback mechanism mediated by cholesterol, a crucial bio-product of the SREBP-activated mevalonate pathway. In this work, we identified acto-myosin contractility and mechanical forces imposed by the extracellular matrix (ECM) as SREBP1 regulators. SREBP1 control by mechanical cues depends on geranylgeranyl pyrophosphate, another key bio-product of the mevalonate pathway, and impacts on stem cell fate in mouse and on fat storage in Drosophila. Mechanistically, we show that activation of AMP-activated protein kinase (AMPK) by ECM stiffening and geranylgeranylated RhoA-dependent acto-myosin contraction inhibits SREBP1 activation. Our results unveil an unpredicted and evolutionary conserved role of SREBP1 in rewiring cell metabolism in response to mechanical cues.
NF-κB non-cell-autonomously regulates cancer stem cell populations in the basal-like breast cancer subtype. Yamamoto M et al. Nature communications 2013

Abstract

Patients with triple-negative breast cancer display the highest rates of early relapse of all patients with breast cancer. The basal-like subtype, a subgroup of triple-negative breast cancer, exhibits high levels of constitutively active NF-κB signalling. Here we show that NF-κB activation, induced by inflammatory cytokines or by epigenetically dysregulated NIK expression, cell-autonomously upregulates JAG1 expression in non-cancer stem cells. This upregulation stimulates NOTCH signalling in cancer stem cells in trans, leading to an expansion of cancer stem cell populations. Among breast cancers, the NF-κB-dependent induction of JAG1 and the NOTCH-dependent expansion of the cancer stem cell population occur only in the basal-like subtype. Collectively, our results indicate that NF-κB has a non-cell-autonomous role in regulating cancer stem cell populations by forming intratumoural microenvironments composed of JAG1-expressing non-cancer stem cells with a basal-like subtype.
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